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To place the modified virus in the right location, Sze and his colleagues injected it directly into an artery leading to the liver. The virus then spread throughout the organ, eventually reaching every cancerous cell. Sze said if he injected the virus into a vein in the arm - or if a cancer patient simply caught a normal cold - only a miniscule amount of virus would reach the tumor. Injecting into the artery, however, concentrates the virus where it is needed.

Once in the liver, the modified virus appears to work by taking advantage of a common genetic defect in cancer cells, specifically infecting those cells while bypassing normal cells. Sze said that in about one-half to two-thirds of all cancers, a protein called p53 is defective. "P53 is like a DNA spell checker," he explained. "If it finds typos, it shuts down replication." And if the typo can't be repaired, p53 commands the cell to commit suicide.

In cancerous cells with a defective p53, the cells continue to divide despite a buildup of harmful mutations - or typos - in the DNA. By releasing the brakes on replication, cancer cells can divide aggressively, but these uncontrolled cells have an Achilles heel, Sze said. P53 would normally prevent the modified virus from entering and replicating. With no p53, these aggressive cancer cells lack a defense against the virus.

While researchers understand how the virus kills cells in a test tube, it's still an open question how it kills cancer cells in human patients, but Sze believes the immune system is involved. The tumors swell after being infected by the virus - a hallmark of immune system involvement - and high levels of immune system hormones appear after treatment. In the next round of trials, Sze hopes to better clarify how the treatment works, along with determining which tumors it most effective
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Contact: Amy Adams
amyadams@stanford.edu
650-723-3900
Stanford University Medical Center
8-Apr-2002